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Cell Host Microbe. 2015 Feb 11;17(2):252-9. doi: 10.1016/j.chom.2015.01.004.

The C-type lectin receptor CLECSF8/CLEC4D is a key component of anti-mycobacterial immunity.

Author information

1
Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, UK.
2
Division of Immunology, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, 792 Cape Town, South Africa.
3
Department of Internal Medicine, Radboud University Medical Center, Nijmegen 6525 GA, the Netherlands.
4
Department of Infectious Diseases, Leiden University Medical Center, Leiden 2333 ZA, the Netherlands.
5
Health Research Unit, Universitas Padjadjaran, Bandung 40161, Indonesia.
6
Division of Anatomical Pathology, University of Cape Town, 7925 Cape Town, South Africa.
7
School of Biosciences, University of Birmingham, Birmingham B15 2TT, UK.
8
Division of Molecular Immunology, Medical Institute of Bioregulation, Kyushu University, Fukuoka 108-8639, Japan.
9
Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, UK; Division of Immunology, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, 792 Cape Town, South Africa. Electronic address: gordon.brown@abdn.ac.uk.

Abstract

The interaction of microbes with pattern recognition receptors (PRRs) is essential for protective immunity. While many PRRs that recognize mycobacteria have been identified, none is essentially required for host defense in vivo. Here, we have identified the C-type lectin receptor CLECSF8 (CLEC4D, MCL) as a key molecule in anti-mycobacterial host defense. Clecsf8-/- mice exhibit higher bacterial burdens and increased mortality upon M. tuberculosis infection. Additionally, Clecsf8 deficiency is associated with exacerbated pulmonary inflammation, characterized by enhanced neutrophil recruitment. Clecsf8-/- mice show reduced mycobacterial uptake by pulmonary leukocytes, but infection with opsonized bacteria can restore this phagocytic defect as well as decrease bacterial burdens. Notably, a CLECSF8 polymorphism identified in humans is associated with an increased susceptibility to pulmonary tuberculosis. We conclude that CLECSF8 plays a non-redundant role in anti-mycobacterial immunity in mouse and in man.

PMID:
25674984
PMCID:
PMC4334100
DOI:
10.1016/j.chom.2015.01.004
[Indexed for MEDLINE]
Free PMC Article

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